scholarly journals Characterization of Neutrophil NADPH Oxidase Activity Reconstituted in a Cell-Free Assay Using Specific Monoclonal Antibodies Raised Against Cytochrome b558

1995 ◽  
Vol 234 (1) ◽  
pp. 208-215 ◽  
Author(s):  
Geraldine Batot ◽  
Cecile Martel ◽  
Nicolas Capdeville ◽  
Frans Wientjes ◽  
Francoise Morel
Keyword(s):  
Monoclonal Antibodies ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Nadph Oxidase Activity ◽  
Cytochrome B558 ◽  
A Cell

scholarly journals Cholesterol: A modulator of the phagocyte NADPH oxidase activity - A cell-free study

Redox Biology ◽  
2014 ◽  
Vol 3 ◽  
pp. 16-24 ◽  
Author(s):  
Rawand Masoud ◽  
Tania Bizouarn ◽  
Chantal Houée-Levin
Keyword(s):  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Nadph Oxidase Activity ◽  
Phagocyte Nadph Oxidase ◽  
A Cell

scholarly journals Regulation of NADPH oxidase activity by Rac GTPase activating protein(s).

1993 ◽  
Vol 4 (11) ◽  
pp. 1217-1223 ◽  
Author(s):  
P G Heyworth ◽  
U G Knaus ◽  
J Settleman ◽  
J T Curnutte ◽  
G M Bokoch
Keyword(s):  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Protein S ◽  
Inhibitory Effect ◽  
Gtpase Activating Protein ◽  
Phagocytic Cells ◽  
Rac Gtpase ◽  
Nadph Oxidase Activity ◽  
A Cell ◽  
Gamma S

Activation of the NADPH oxidase of phagocytic cells requires the action of Rac2 or Rac1, members of the Ras superfamily of GTP-binding proteins. Rac proteins are active when in the GTP-bound form and can be regulated by a variety of proteins that modulate the exchange of GDP for GTP and/or GTP hydrolysis. The p190 Rac GTPase Activating Protein (GAP) inhibits human neutrophil NADPH oxidase activity in a cell-free assay system with a K1 of approximately 100 nM. Inhibition by p190 was prevented by GTP gamma S, a nonhydrolyzable analogue of GTP. Similar inhibition was seen with a second protein exhibiting Rac GAP activity, CDC42Hs GAP. The effect of p190 on superoxide (O2-) formation was reversed by the addition of a constitutively GTP-bound Rac2 mutant or Rac1-GTP gamma S but not by RhoA-GTP gamma S. Addition of p190 to an activated oxidase produced no inhibitory effect, suggesting either that p190 no longer has access to Rac in the assembled oxidase or that Rac-GTP is not required for activity once O2- generation has been initiated. These data confirm the role of Rac in NADPH oxidase regulation and support the view that it is the GTP form of Rac that is necessary for oxidase activation. Finally, they raise the possibility that NADPH oxidase may be regulated by the action of GAPs for Rac proteins.

scholarly journals Neuroprotective Benefits of Exercise and MitoQ on Memory Function, Mitochondrial Dynamics, Oxidative Stress, and Neuroinflammation in D-Galactose-Induced Aging Rats

2021 ◽  
Vol 11 (2) ◽  
pp. 164
Author(s):  
Jae-Hoon Jeong ◽  
Jung-Hoon Koo ◽  
Jang Soo Yook ◽  
Joon-Yong Cho ◽  
Eun-Bum Kang
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Cognitive Impairment ◽  
Nadph Oxidase ◽  
Learning And Memory ◽  
Oxidase Activity ◽  
Mitochondrial Dynamics ◽  
Nadph Oxidase Activity ◽  
Aging Rats ◽  
Positive Effects

Exercise and antioxidants have health benefits that improve cognitive impairment and may act synergistically. In this study, we examined the effects of treadmill exercise (TE) and mitochondria-targeted antioxidant mitoquinone (MitoQ), individually or combined, on learning and memory, mitochondrial dynamics, NADPH oxidase activity, and neuroinflammation and antioxidant activity in the hippocampus of D-galactose-induced aging rats. TE alone and TE combined with MitoQ in aging rats reduced mitochondrial fission factors (Drp1, Fis1) and increased mitochondrial fusion factors (Mfn1, Mfn2, Opa1). These groups also exhibited improved NADPH oxidase activity and antioxidant activity (SOD-2, catalase). TE or MitoQ alone decreased neuroinflammatory response (COX-2, TNF-α), but the suppression was greater with their combination. In addition, aging-increased neuroinflammation in the dentate gyrus was decreased in TE but not MitoQ treatment. Learning and memory tests showed that, contrarily, MitoQ alone demonstrated some similar effects to TE but not a definitive improvement. In conclusion, this study demonstrated that MitoQ exerted some positive effects on aging when used as an isolated treatment, but TE had a more effective role on cognitive impairment, oxidative stress, inflammation, and mitochondria dysfunction. Our findings suggest that the combination of TE and MitoQ exerted no synergistic effects and indicated regular exercise should be the first priority in neuroprotection of age-related cognitive decline.

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